Evidence map›Paper›PMID 11857084›Full record

ArticleOncogene2002

Adenovirus E1A requires the yeast SAGA histone acetyltransferase complex and associates with SAGA components Gcn5 and Tra1.

Caroline A Kulesza, Heather A Van Buskirk, Michael D Cole, Joseph C Reese, M Mitchell Smith, Daniel A Engel

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Analysis of Gal4-directed transcription activation using Tra1 mutants selectively defective for interaction with Gal4.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Caroline A KuleszaDepartment of Microbiology and Cancer Center, University of Virginia School of Medicine, Charlottesville, Virginia, VA 22908, USA.
Heather A Van Buskirk
Michael D Cole
Joseph C Reese
M Mitchell Smith
Daniel A Engel
University of Virginia · USPrinceton University · USPennsylvania State University · US

Funding

TRAINING IN CELL AND MOLECULAR BIOLOGYT32GM008136 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI STUKENBERG, P. TODD · 1985 to 2020
$8.5M
REGULATION OF DNA DAMAGE INDUCED GENES BY YEAST TAFIISR01GM058672 · NIGMS · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI REESE, JOSEPH C · 1999 to 2019
$6.5M
HISTONE GENE EXPRESSION IN YEASTR01GM028920 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI SMITH, M MITCHELL · 1985 to 2007
$2.7M
ADENOVIRUS E1A PROTEIN AND THE SWI/SNF COMPLEXR01CA060675 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI ENGEL, DANIEL A · 2001 to 2005
$1.1M
CHROMATIN TARGETS FOR CANCER THERAPYR01CA087620 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI ENGEL, DANIEL A · 2000 to 2002
$784k
ADENOVIRUS 243R E1A PROTEIN AND CELLULAR TRANSCRIPTIONR29CA060675 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI ENGEL, DANIEL A · 1995 to 1999
–
NCI NIH HHS CA60675NCI NIH HHS CA87620NIGMS NIH HHS 5T32GM08136NIGMS NIH HHS GM28920NIGMS NIH HHS R01 GM028920NIGMS NIH HHS R01 GM058672
6 · The paper itself

Abstract

The budding yeast Saccharomyces cerevisiae was used as a model system to study the function of the adenovirus E1A oncoprotein. Previously we demonstrated that expression of the N-terminal 82 amino acids of E1A in yeast causes pronounced growth inhibition and specifically interferes with SWI/SNF-dependent transcriptional activation. Further genetic analysis identified the yeast transcription factor Adr1 as a high copy suppressor of E1A function. Transcriptional activation by Adr1 requires interaction with co-activator proteins Ada2 and Gcn5, components of histone acetyltransferase complexes including ADA and SAGA. Analysis of mutant alleles revealed that several components of the SAGA complex, including proteins from the Ada, Spt, and Taf classes were required for E1A-induced growth inhibition. Growth inhibition also depended on the Gcn5 histone acetyltransferase, and point mutations within the Gcn5 HAT domain rendered cells E1A-resistant. Also required was SAGA component Tra1, a homologue of the mammalian TRRAP protein which is required for c-myc and E1A induced cellular transformation. Additionally, Gcn5 protein could associate with E1A in vitro in a manner that depended on the N-terminal domain of E1A, and Tra1 protein was co-immunoprecipitated with E1A in vivo. These results indicate a strong requirement for intact SAGA complex for E1A to function in yeast, and suggest a role for SAGA-like complexes in mammalian cell transformation.

Indexed as

TATA-Binding Protein Associated FactorsTranscription Factor TFIIDAcetyltransferasesAdaptor Proteins, Signal TransducingAdenovirus E1A ProteinsDNA-Binding ProteinsFungal ProteinsGenes, FungalHistone AcetyltransferasesMultienzyme Complexesp300-CBP-Associated FactorProtein BindingProtein KinasesProtein Structure, TertiaryRNA, MessengerSaccharomyces cerevisiaeAcetyltransferasesADA2 protein, S cerevisiaeAdaptor Proteins, Signal TransducingAdenovirus E1A ProteinsADR1 protein, S cerevisiaeDNA-Binding ProteinsFungal ProteinsGCN5 protein, S cerevisiaeHFI1 protein, S cerevisiaeHistone AcetyltransferasesMultienzyme ComplexesNGG1 protein, S cerevisiaep300-CBP-Associated FactorProtein KinasesRNA, MessengerSaccharomyces cerevisiae ProteinsTAF5 protein, S cerevisiaeTATA-Binding Protein Associated FactorsTrans-ActivatorsTranscription FactorsTranscription Factor TFIID

Identifiers

PMID11857084
OpenAlexW2333928527

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.